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uWORLD Cardio Pathophysiology

Terms in this set (280)

Urinary 5-hydroxyindolearcretic acid

> Carcinoid syndrome typically presents with episodic flushing, secretary diarrhea and wheezing. It can lead to pathognomonic plaque-like deposits of fibrous tissue on the right-sided endocardium, causing tricuspid regurgitation and right-sided heart filature. Elevated 24 hour urnary 5-hydroxyindoleacetic acid can confirm the diagnosis.

> The autospy findings - endocardial thickening and fibrosis of tricuspid and pulmonary valves - are chracerstic of carcinoid heart disease.. Carcinoids are well-differentiated neuroendocrine turbos found most commonly in the distill small intestine and proximal colon, with a strong propensity for metastasis to the liver. These tumors secrete seers products (including histamine, serotonin, and vasoactive intestinal peptide) that are metabolized in the liver. In patients with liver metastasis, these hormones are relased directly into the systemic circulation, leading to carcinoid syndrome.

> Carcinoid heart diseases is caused by excessive secretion of serotonin, which stimulates fibroblast growth and fibrognesis. Pathognomic plaque-like deposits of fibrous tissue occur most commonly on the endocardium, leading to tricuspid regurgitation, pulmonic valvulpathy, and right-sided heart failure )eg ascites, peripheral edema). Endocardial fibrosis and thickening are generally limited to the right heart as vasoactive products and inactivated distally by pulmonary vascular endothelial monoamine oxidase.

- Measuring of plasma cortisol: Used for diagnosing adrenal insufficiency and Crushing syndrome

- Measuring of homocysteine: elevation may contribute to arterial and venous thrombosis and to the development of atherosclerosis.

- Measuring of plasma phenylalanine: May be elevated in patients with phenylalanine hydroxylase deficiency, resulting in central nervous system damage/intellectual disability :

- Measuring of porphobilinogen: May be elevated in the porphyria, which are caused by deficiencies of the heme synthesis enzymes. The porphyries may produce cutaneous lesions, skin photosensitivity, or attacks of abdominal pain and neurological disturbances (acute intermittent porphyria)

- Measuring of vanillymandelic acid: by product of norepinephrine and epinephrine, and can be used to detect neuroblastoma and other tumors of neural crest origin
Profound hypotension

> Rupture of the left ventricular free wall is a catastrophic mechanical complication of anterior wall myocardial infarction (MI) that usually occurs within the first 5-14 days after MI. Rupture leads to hemoperricardium and cardiac tamponade, causing profound hypertension and shock with rapid progression to pulseless electrical activity and death.

> This patient most likely died from profound hypotension due to ruptured left ventricular free wall. Her initial presentation of substernal chest discomfort and ST segment elevation in anterior precordial leads in consistent with acute anterior wall myocardial infarction (MI). Free wall rupture is a catastrophic mechanical complication that usually occurs within the first 5-14 days after a large anterior transmural MI (from left anterior descending occlusion). During this timeframe, the infarcted myocardium is substantially weakened by coagulative necrosis, neutrophilic and macrophage infiltration, and enzymatic lysis of myocardial connective tissue. Abrupt rupture of the left ventricle leads to hemopericardium and cardiac tamponade. Patients have sudden onset of chest pain and profound hypotension and shock, with rapid progression to pulseless electrical activity and death.

> Carotid artery occlusion = can lead to ischemic symptoms (hemiparesis, vision changes) but does not typically cause sudden death.
> Hypertensive emergency can lead to aortic dissection = that typically presents with tearing chest or back pain. Hypertension and shock can occur with retrograde extension of the dissection into he pericardial cavity or contrary arteries, with resultant hemoperricardium or MI, respectively. However, this patient's presentation of intimal normal blood pressure and ST segment elevation is more suggestive of acute MI with subsequent cardiac rupture.
Isosorbide dinitrate

> This patient's presentation, family history of premature sudden death, and systolic mummer that accentuates with standing from a supine position is consistent with hypertrophic cardiomyopathy (HCM). Patients with HCM have dynamic left ventricular outflow tract (LVOT) obstruction that worsens with decreased left ventricular (LV) volume (as can be caused by decreased preload and/or reduced systemic vascular resistance). As such, medications that generally should be avoided in patients with HCM include:
--> Vasodilators (eg dihydropyridine calcium channel blockers, nitroglycerin, and ACE inhibitors) decrease systemic vascular resistance, leading to decreased after load and lower LV volumes.
--> Diuretics decrease LV venous filing (preload) and also result in greater outflow obstruction.

In contrast, negative inotropic agents such as beta blockers (metoprolol), nondihydropyridine calcium channel blockers (verapamil), and disopyramide Reduce LVOT obstruction and are helpful in symptomatic patients with HCM. In addition, beta blockers may also help reduce anginal symptoms by decreasing myocardial oxygen demand.

> The dynamic left ventricular (LV) outflow tract obstruction that occurs in hypertrophic cardiomyopathy worsens with decreased LV volume, which can be caused by education in cardiac preload and/or after load. Therefore, medications that decrease venous return or systemic vascular resistance (dihydropyridine calcium channel blockers, nitroglycerin) should generally be avoided.

> Fenoldopam is a short-acting, elective, peripheral dopamine-1 receptor agonist with little to no effect on alpha- or beta-adrenergic receptors. Dopamine-1 receptor stimulation activates adennylyl cyclase and raises intracellular cyclic AMP, resulting in vasodilation of most arterial beds with a corresponding decrease in systemic blood pressure. Renal vasodilation is particularly prominent and leads to *increase renal perfusion, diuresis, and natriuresis. This makes fenoldopam especially beneficial in patients with acute kidney injury.

> Esmolol is a short-acting cardioselective beta-1 receptor antagonist. It works by reducing heart rate and myocardial contractility. Esmolol is not a vasodilator and does not increase renal perfusion.

> Hydrazine is a direct arteriolar vasodilator with no significant therapeutic effect on renal perfusion or natriuresis. It is not often in hypertensive emergency as it is associated wth reflex sympathetic activation, resulting in increased heart rate and contractility along with sodium and fluid retention.

> Nitroglycerin is a rapid-acting ventilator that decreases preload and cardiac output. It does NOT cause arterial dilation and does NOT improve renal perfusion. Nitroglycerin is primarily used to reduce myocardial oxygen demand in acute coronary syndrome.
> Phenylephrine is an alpha-adrenergic agonist that causes an increase in systemic vascular resistance due to arterial vasoconstriction. It is used in patients with hypotension or shock and is contraindicated in hypertensive emergency.
Coronary arteriolar dilation

> In coronary artery disease, coronary vessel occlusion can be bypassed by the natural existence of compensatory recruitment of collateral vessels that help support blood flow. These collateral micro vessels from a network of passageways between major vessels, allowing supplemental blood flow to myocardium distal to an occluded vessel. In the presence of myocardial ischemia, coronary arterioles vasodilator in response to local mediators, diverting collateral blood flow to ischemic areas. Thus, collateral circulation helps to alleviate ischemia and preserve myocardial function.

>Drugs such as adenosine and dipyridamole and selective vasodilators of coronary vessels. When myocardial ischemia is present, these drugs cause a redistribution of blood flow through the collateral micro vessels and coronary arterioles that can reduce collateral blood flow. Arterioles within ischemic areas are already maximally dilated prior to drug administration. However, use of these agents cause vasodilation of canary arterioles in nonischemic regions. This leads to decreased perfusion pressure within the collateral micro vessels supplying the ischemic myocardium, diverting blood flow from ischemic areas to nonischemic areas. This phenomena, known as coronary steal, may lead to hypo perfusion and potential worsening of existing ischemia.

> Collateral micro vessels from adjacent pathways for blood flow to areas distal to an occluded vessel. Adenosine and dipyridamole are selective vasodilators of canary vessels that can cause coronary steal, a phenomenon in which blood flow in ischemic ares is reduced due to arteriolar vasodilation in nonischemic areas. Coronary steal can lead to hypo perfusion and worsening of existing ischemia.

> Common side effects of nondihydropyridine calcium channel blockers (eg. dilitizaem, verapamil) include constipation, bradycardia, atrioventricular conduction block (negative chronotropic effect), and worsening of heart failure in patients with reduced left ventricular function (negative inotropic effect)

> Beta blockers (BBs) are commonly used used for heart rate control in patients with AF and can cause or worsen AV block. Nonselective BBs (propranolol) impair bronchodilation and are contraindicated in patients with asthma and/or severe chronic obstructive pulmonary disease.. In addition, constipation is not a significant side effect of BB therapy.

> This patent's presentation (constipation, new-onset second-degree atrioventricular [AV] block, and syncope) in the setting of new medication use atrial fibrillation (AF) is likely due to calcium channel blocker (CCB) therapy. Diltiazem and verapamil are nondihydrophyridine CCBs that are frequently used for hypertension, angina pectoris, and supra ventricular arrhythmias (atrial flutter, AF, paroxysmal supraventircular tachycardia).

> These drugs exert their primary action by blocking the L-type calcium channels, thereby decreasing phase 0 depolarization and conduction velocity in the sinoatiral and AV nodes. This leads to slowing of the sinus rate and conduction through the AV node, which can then cause bradycardia and varying degrees of AV block. The drugs also have a negative inotropic effect and are relatively contraindicated in patients with congestive heart failure due to left ventricular systolic dysfunction. Constipation is a major side effect nondihydropyridines CCBs (verapamil > diltiazem)